Accelerated idioventricular rhythm as a manifestation of chronic renocardiac syndrome: A case report

Abstract In this case report, we describe a patient who presented with chronic symptoms and signs of uremia and persistent accelerated idioventricular rhythm (AIVR) on electrocardiogram. Findings from blood tests, echocardiography, renal ultrasound, and renal scan were suggestive of heart failure with reduced ejection fraction and chronic kidney disease, and attendance of daily hemodialysis sessions led to the restoration of sinus rhythm. Typically, AIVR has a favorable prognosis and, if necessary, medical intervention focuses on addressing the underlying responsible causes. Accumulation of uremic toxins has the potential to trigger the formation of AIVR and clearance of small solutes through conventional hemodialysis may contribute to sinus rhythm restoration.

Transthoracic echocardiography showed a left ventricle with normal size, severe global hypokinesia, and an estimated ejection fraction of 25%-30%.Right ventricle had normal size but impaired systolic function as well.Moreover, there was mild biatrial enlargement, mild tricuspid, and mitral valve regurgitation and aortic valve sclerosis.Renal ultrasound revealed small sized kidneys, no renal pelvis dilatation, thin and hyperechogenic parenchyma, and loss of corticomedullary differentiation.Furthermore, a 99m Tc-MAG 3 renal scan was performed that showed decreased renal perfusion, radionuclide uptake, and excretion of both kidneys, while there was no blockage of urine flow.
The patient met multiple criteria that warranted the start of longterm hemodialysis treatment (sustained and severely reduced eGFR, bleeding diathesis, pruritus, volume overload refractory to high doses of diuretics, deteriorating nutritional status, and persistent fatigue) so a Cardiorenal Interdisciplinary Team meeting was called that favored this decision.Despite the abnormal ECG, there was absence of hemodynamic significance, so a dialysis catheter was placed and he attended conventional intermittent hemodialysis sessions.It is noteworthy that, due to the patient's normal urine output, dialysis sessions were conducted with an emphasis on diffusion with minimal ultrafiltration volume.
Next day, the patient underwent his second dialysis session while still maintaining AIVR.On Day 3, a new dialysis session was performed, and a new ECG showed restoration of sinus rhythm with salvos of premature ventricular complexes originating from the same ventricular focus (Figure 2).The following day, there was complete restoration of sinus rhythm on ECG (Figure 3).An invasive coronary angiography was performed that revealed a chronic three-vessel disease.The patient was discussed at the Heart Team meeting, and coronary artery bypass graft surgery was decided as the optimal method of revascularization.On Day 5, the patient had his final dialysis session during his inpatient hospital stay, while maintaining sinus rhythm, and his left ventricular ejection fraction was mildly improved (LVEF 30%-35%).After being introduced to the hospital's hemodialysis schedule, he was discharged with significant clinical improvement.

F I G U R E 1 ECG tracing on admission
showing AIVR and a capture beat.

TA B L E 1
Patient's basic metabolic panel.On follow-up visit, the patient had complete remission of his symptoms.ECG tracing showed normal sinus rhythm.He had enrolled a hemodialysis program with three sessions per week while being on a waiting list for elective coronary artery bypass surgery.
Lastly, an Implantable Cardioverter-Defibrillator implantation was proposed with the purpose of primary prevention.

| DISCUSS ION
To the best of our knowledge, it is described for the first time in this report a case of a non-dialysis patient with advanced CKD who presented with persistent AIVR that was restored to sinus rhythm after initiation of daily hemodialysis sessions.AIVR is a rare arrhythmia characterized by three or more consecutive beats originating from a ventricular focus at a rate between 50 and 110 bpm.It is most commonly observed after reperfusion of an acute myocardial infarction; however, it has been documented in cases with drug intoxications (e.g., digoxin, beta agonists, and anesthetic agents), electrolyte disturbances, cardiomyopathies (e.g., hypertrophic, dilated, and arrhythmogenic), and in healthy individuals without any underlying cardiac pathology (Riera et al., 2010).It is important to note that typically AIVR has a favorable prognosis and, if necessary, medical intervention focuses on addressing the underlying responsible causes (Bijsterveld et al., 2022).It can be easily postulated that in our case report, chronic uremic state was the trigger for AIVR formation.
It is well-established that multiple interactions exist between heart and kidneys and cardiovascular disease (CVD) often leads to kidney injury through a cascade of neurohormonal, hemodynamic, and inflammatory mechanisms.These pathophysiological interactions gave birth to the so-called cardiorenal syndrome (Ronco et al., 2008).Nevertheless, the heart-kidney relationship is bidirectional as CKD is a strong risk factor for adverse cardiovascular events (Kingma Jr. et al., 2015).CKD-related CVD accounts for almost 50% of all-cause mortality in CKD patients and manifests in clinical practice mainly as coronary artery disease, stroke, heart failure, and arrhythmias (Tonelli et al., 2016).Regarding the latter, CKD patients are vulnerable to heart rhythm disorders and exhibit an increased burden of supraventricular (especially atrial fibrillation) and ventricular tachyarrhythmias, and sudden cardiac death (SCD) (Turakhia et al., 2018).
The probability of SCD is inversely related to eGFR, but SCD is a leading cause of death even in young patients in the early stages of CKD, suggesting mechanisms other than ischemia.Increased predilection for ventricular arrhythmias and SCD in CKD patients seems to stem from complex processes closely related to metabolic disarrangements secondary to renal dysfunction, in contrary to individuals with normal kidney function in which acute coronary syndrome, systolic heart failure, and myocardial scars are the usual pathological substrate (Bonato & Canziani, 2017;Tonelli et al., 2016).
In particular, uremic solutes that are inadequately excreted or metabolized due to diminished renal function, but remain biologically active, are termed uremic toxins (UTs).UTs tend to accumulate with subsequent catastrophic consequences on virtually all organ systems.Based on their physicochemical properties and the ability of conventional hemodialysis to remove them, UTs are most commonly classified into small UTs (molecular weight ≤500 Da), middle UTs (molecular weight >500 Da), and protein-bound UTs (Moradi et al., 2013).Whereas small UTs are freely filtered, a great proportion of middle and protein-bound UTs are difficult to remove via conventional low-flux hemodialysis membranes and their gradual build-up is considered a strong non-traditional risk factor for CVD in hemodialysis-dependent patients (Moradi et al., 2013).Actually, considerable emphasis has been placed on unfiltered compounds such as fibroblastic growth factor-23, indoxyl sulfate, and p-cresyl sulfate.In pre-dialysis stages, however, the accumulation of small UTs exerts harmful biological activity on the myocardium as well (Lekawanvijit, 2018).This is clearly highlighted in our case report in which small UTs clearance through the first hemodialysis sessions led to an immediate reduction of arrhythmia burden, putting a halt to the vicious cycle of renocardiac syndrome.
Enhanced automaticity and triggered activity initiated by afterdepolarizations in ventricular fibers are two mechanisms that are most consistent with AIVR formation in a vulnerable myocardium under the cumulative impact of small UTs (Antzelevitch & Burashnikov, 2011;Hsueh et al., 2014).Arrhythmia could allegedly be either considered a coincidental finding or attributed to ischemic heart disease.Still, the fact that sinus rhythm recovery was achieved through diffusive dialysis sessions with low ultrafiltration volume, while no other intervention was made, suggests that the uremic milieu is responsible.
There is a crucial knowledge gap in the understanding of the codependent relationship between the heart and the kidneys.This gap becomes more evident in regard to arrhythmias formation and SCD in CKD patients (Boriani et al., 2015).While their role is increasingly recognized, the involvement of UTs, especially of those with low molecular weight, in cardiac electrophysiological remodeling and the underlying molecular mechanisms are incompletely understood and need to be further evaluated in experimental studies (van Ham et al., 2022).Advances in hemodialysis techniques by using all available membrane separation processes and introducing novel dialysis membranes that allow the clearance of middle, large, and even protein-bound UTs will also assist in this direction.

AUTH O R CO NTR I B UTI O N S
KD conception, initial draft and completion of manuscript.GE, PC and VV review and revisions to manuscript.

CO N FLI C T O F I NTE R E S T S TATE M E NT
There is no conflict of interest.

DATA AVA I L A B I L I T Y S TAT E M E N T
The data that support the findings of this study are available from the corresponding author upon reasonable request.

E TH I C S S TATEM ENT
All the procedures were conducted according to the principles of the Helsinki Declaration.

CO N S E NT
Written informed consent has been obtained from the patient in line with COPE guidelines.

F
I G U R E 2 ECG showing sinus rhythm with salvos of premature ventricular complexes on day 3. F I G U R E 3 ECG showing complete restoration of sinus rhythm before discharge.